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Farmer's Lung

  • Author: Laurianne G Wild, MD, FAAAAI, FACAAI; Chief Editor: Zab Mosenifar, MD, FACP, FCCP  more...
 
Updated: Dec 21, 2015
 

Background

Farmer's lung is a type of hypersensitivity pneumonitis. Hypersensitivity pneumonitis, also known as extrinsic allergic alveolitis, is an immunologically mediated inflammatory disease of the lung involving the terminal airways. The condition is associated with intense or repeated exposure to inhaled biologic dusts. The classic presentation of farmer's lung results from inhalational exposure to thermophilic Actinomyces species and occasionally from exposure to various Aspergillus species.

The effect of these antigens in farmers was described as early as 1713. In Britain in 1932, Campbell described a disorder of the lung caused by inhalation of dust from moldy hay. In 1964, Ramazzini and Wright[1] described workers getting "diseases of the chest."

Thermophilic actinomycetes species include Saccharopolyspora rectivirgula (formerly Micropolyspora faeni), Thermoactinomyces vulgaris, Thermoactinomyces viridis, and Thermoactinomyces sacchari, among others.[2] These organisms flourish in areas of high humidity and prefer temperatures of 40-60°C.

The thermophilic actinomycetes are ubiquitous organisms usually found in contaminated ventilation systems and in decaying compost, hay, and sugar cane (bagasse). Exposure to large quantities of contaminated hay is the most common source of inhalational exposure for farmers who develop farmer's lung; therefore, grain farmers are not at risk for the development of the disease. Farmer's lung is often a disease of dairy farmers who handle contaminated hay during the winter months. Most cases of farmer's lung occur in cold, damp climates in late winter and early spring when farmers use stored hay to feed their livestock.

Exposure to the causative antigens depends on the type of farming, industry, and climate in the area. Note that farming practices are changing with time and that new antigens may be introduced or disappear from a region (eg, the disappearance of bagassosis in Louisiana sugar cane workers,[3] the appearance of Pseudomonas fluorescens in machine operator's lung). The dynamic nature of this disease and the changing environment may lead to new challenges for the clinician.

In addition to the inhalational exposure to the organic dusts responsible for the hypersensitivity reaction in farmer's lung disease, allergens, chemicals, toxic gases, and infectious agents must also be considered as potential triggers of airway symptoms in symptomatic farmers. Farming is currently ranked as one of the top 3 most hazardous occupations, along with construction and mining.[4, 5]

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Pathophysiology

The pathogenesis of farmer's lung depends on the intensity, frequency, and duration of exposure and on host response to the causative antigen. Both humoral and cell-mediated immune responses seem to play a role in pathogenesis. During acute episodes, acute neutrophilic infiltration is followed by lymphocytic infiltration of the airways. Levels of interleukins 1 and 8 and tumor necrosis factor-alpha are increased.[6] These cytokines have proinflammatory and chemotactic properties. They cause the recruitment of additional inflammatory mediators, resulting in direct cellular damage and changes in the complement pathway, which provide the necessary stimuli to increase vascular permeability and migration of leukocytes to the lung.[7, 8]

If the acute exposure is large, a dramatic increase in inflammation leads to increased vascular permeability, which can alter the alveolar capillary units, thus promoting hypoxemia and decreased lung compliance. If the exposure is prolonged and continuous, collagen deposition and destruction of the lung parenchyma occur with resultant decreased lung volumes.

Strong evidence suggests the involvement of immune complex–induced tissue injury (type III hypersensitivity). The timing of development of symptoms after exposure supports this conclusion. The presence of antigen-specific immunoglobulin and complement activation and deposition in the lung also supports immune-complex or type III hypersensitivity in the pathogenesis of farmer's lung.

Cell-mediated, delayed-type hypersensitivity (type IV hypersensitivity) also plays a major role in the pathogenesis of this syndrome. The presence of lymphocytes, macrophages, and granulomas in the alveolar spaces and the interstitium supports this conclusion.

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Epidemiology

Frequency

United States

Farmer's lung is one of the most frequent types of hypersensitivity pneumonitis. Note the following:

  • Incidence is highly variable and depends on multiple factors, such as intensity, frequency, and duration of exposure, type of farming, and climate.
  • An incidence of 8-540 cases per 100,000 persons per year for farmers has been reported.
  • Hypersensitivity pneumonitis affects 0.4-7% of the farming population.
  • In a 2007 study in the United States, farmer's lung accounted for 11% of cases of hypersensitivity pneumonitis. [9]

International

The prevalence of farmer's lung in the United Kingdom has been reported to be 420-3000 cases per 100,000 at-risk persons. Note the following:

  • Epidemiologic surveys in France [10] and Sweden [11] show a cumulative prevalence of the disease in the range of 2.5-153 cases per 1000 farmers.
  • Incidence of farmer's lung in Finland is 0.7%. This figure is calculated from death certificates. [12]
  • As reported in 2006, farmer's lung appears to be on the decline, at least in some parts of the world. Specifically, the incidence of farmer's lung in Ireland declined from 1997-2002. [13] Effective changes in farming practice and an increase in awareness of the disease has contributed to this decline.

Mortality/Morbidity

The mortality rate from farmer's lung is reportedly 0-20%. Note the following:

  • Death usually occurs 5 years after diagnosis.
  • Several factors have been shown to increase mortality rates in farmer's lung, including clinical symptoms occurring more than 1 year before diagnosis, symptomatic recurrence, and pulmonary fibrosis at the time of diagnosis.
  • Comorbid factors: Although a history of smoking appears to decrease the overall risk for the development of hypersensitivity pneumonitis, a smoking history is the strongest predictor of increased respiratory symptoms once the diagnosis is made. Preexisting bronchial hyperreactivity with airway obstruction is also a factor.
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Contributor Information and Disclosures
Author

Laurianne G Wild, MD, FAAAAI, FACAAI Chief and Professor of Clinical Medicine, Section of Clinical Immunology, Allergy and Rheumatology, Director, Allergy and Immunology Fellowship Training Program, Tulane University School of Medicine; Director, Allergy and Immunology Clinic, Southeast Louisiana Veterans Health Care System of New Orleans

Laurianne G Wild, MD, FAAAAI, FACAAI is a member of the following medical societies: Alpha Omega Alpha, American Academy of Allergy Asthma and Immunology, American College of Allergy, Asthma and Immunology, Association of Subspecialty Professors

Disclosure: Nothing to disclose.

Coauthor(s)

Eduardo E Chang, MD Fellow, Department of Allergy and Immunology, Tulane University

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Zab Mosenifar, MD, FACP, FCCP Geri and Richard Brawerman Chair in Pulmonary and Critical Care Medicine, Professor and Executive Vice Chairman, Department of Medicine, Medical Director, Women's Guild Lung Institute, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD, FACP, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Thoracic Society

Disclosure: Nothing to disclose.

Additional Contributors

Sat Sharma, MD, FRCPC Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, World Medical Association

Disclosure: Nothing to disclose.

Acknowledgements

Gregg T Anders, DO Medical Director, Great Plains Regional Medical Command , Brooke Army Medical Center; Clinical Associate Professor, Department of Internal Medicine, Division of Pulmonary Disease, University of Texas Health Science Center at San Antonio

Disclosure: Nothing to disclose.

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